ArticleJournal of orthopaedic surgery and research2025
The impact of miR-221-3p modification by the m6A demethylase ALKBH5 on the inflammatory response in spinal tuberculosis and its diagnostic significance.
Article in Journal of orthopaedic surgery and research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundThe interplay between N6-methyladenosine (m6A) modification and microRNAs (miRNAs) in the pathogenesis of spinal tuberculosis (STB) remains incompletely understood. This study aimed to investigate the regulatory mechanism involving the m6A demethylase ALKBH5 and specific miRNAs in STB.
methodsmiRNA sequencing was conducted to identify differentially expressed miRNAs in STB tissues. The expression levels of miR-221-3p and ALKBH5 were validated via qRT-PCR in tissue samples and peripheral blood from 50 STB patients and healthy controls. The diagnostic potential of these biomarkers was assessed using ROC curve analysis. The expression of ALKBH5 and miR-221-3p was assessed by qRT-PCR, immunohistochemistry (IHC), and immunofluorescence. ALKBH5-mediated m6A modification of pri-miR-221-3p was analyzed by methylated RNA immunoprecipitation (MeRIP) Functional effects on inflammatory responses were evaluated by measuring TNF-α, IL-1β, and IL-6 levels following functional experiments, combined with ELISA assays.
resultsmiR-221-3p was significantly downregulated in STB tissues, peripheral blood, and BCG-infected macrophages, indicating its potential as a diagnostic marker. In contrast, ALKBH5 expression was upregulated. Functionally, knockdown of miR-221-3p increased the production of pro-inflammatory cytokines and exacerbated inflammation, whereas its overexpression had the opposite effect. Mechanistically, ALKBH5 was found to directly demethylate pri-miR-221-3p, as confirmed by MeRIP, thereby impairing its maturation. Silencing ALKBH5 restored miR-221-3p expression and reduced cytokine secretion.
conclusionmiR-221-3p may serve as a potential diagnostic biomarker for STB. ALKBH5 upregulation promotes STB progression by inhibiting miR-221-3p maturation via m6A demethylation, which enhances the inflammatory response. Targeting the ALKBH5/miR-221-3p axis may offer a novel therapeutic approach for STB.
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